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Plague |
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Causative Agent |
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Bacterial
disease caused by infection with Yersinia pestis, causing an acute infection and high mortality rates in mammals.
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Plague is a flea-transmitted disease affecting and perpetuated by rodents.
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This same
bacteria caused three human
epidemics in recorded history; today, wildlife act as
reservoirs for the
bacteria throughout the world in semi-arid areas on every continent except Australia and Antarctica.
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Distribution |
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Geographic:
Seasonality:
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Click on the diagram to enlarge. |
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Plague cycles can occur through both wildlife and in urban areas. |
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Hosts, Transmission and Life Cycle |
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Hosts:
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Y. pestis
bacteria are maintained in a complex cycle involving rodents and fleas.
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Infected fleas tend to remain in burrows for prolonged periods, hence, burrowing rodents, their predators and animals that share similar habitats as burrowing rodents will often have high rates of infection when compared to other species.
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“Spill-over” from rodents to other species often results in outbreaks or
“epizootics”.
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Rabbits, carnivores, primates and birds are generally not involved in cycles, although they may occasionally aid in spreading infectious fleas or prey.
Transmission
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Transmission of
bacteria usually occurs via a flea bite – blood-borne
bacteria from the infected animal, remaining in the
gastrointestinal tract of the flea, is transferred when the flea begins its blood meal from its next uninfected host.
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Less commonly, upon ingestion of tissues of infected animal, a predator/scavenger can become infected. Sharp objects, such as bones, may puncture tissues of the mouth and throat thereby enabling entry of the
bacteria.
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Rarely, through inhalation of aerosolized
bacteria.
Life Cycle:
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Signs and Symptoms |
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Observation of
clinically affected wild mammals is unlikely. The discovery of dead animals is more common.
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Lesions
vary according to the mode of transmission and susceptibility of the host.
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Accordingly, symptoms of animals that have contracted plague will vary from:
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swollen lymph nodes near site of inoculation (flea bites, oral punctures)
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abscess
formation near site of inoculation (flea bites, oral punctures)
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muscle soreness
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loss of appetite
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fever
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depression
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necrosis
of
lymph tissue
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edema
in the lungs
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death may occur rapidly before the appearance of
clinical symptoms
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A history of rapid, large declines of colonial rodents is suggestive of plague.
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confirmation requires submission of samples to an appropriate diagnostic laboratory
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Three types of plague possible in susceptible non-rodent mammal species:
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Bubonic
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initially characterized by swelling (from the Latin bubo = swelling) of tissues around the flea bite
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replication of the
bacteria occurs, and in this type of plague, is restricted to the
lymph nodes that drain the site of the flea-bite, often producing
hemorrhage and localized
necrosis of affected nodes
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Septicemic
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defined by
bacteria in the blood without the presence of buboes. Results from ingestion of infected prey or through the bites from infected animals
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lesions
are typically first observed in the liver and spleen
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coagulation of blood within vessels, escape of blood from vessels into surrounding tissues,
hemorrhage, and blood clotting may cause a dark, reddish-black discolouration of tissues visible under the skin – leading to the name “black death”
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bacteria
in blood may spread to lungs leading to
pneumonic form of disease
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Pneumonic
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inhalation of aerosolized droplets (mist) containing
bacteria
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often fatal
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Meat Edible? |
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Human infection has been reported from contact with recently dead animals (e.g., dressing/skinning).
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If you suspect an animal has been infected with plague
DO NOT CONSUME ANY MEAT and contact the nearest
Health Authority.
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Human Health Concerns and Risk Reduction |
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Plague is a potentially deadly
zoonotic disease and precautions should be taken when an animal suspected of having plague is encountered.
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Symptoms in humans include:
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acute onset of fever
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swollen/painful
lymph nodes
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general malaise
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Septicemic
and
pneumonic plague in humans are most serious: characterized by fever, prostration, coughing, respiratory distress –
shock,
hemorrhage and death may follow.
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Viable Y. pestis
bacteria have also been isolated from soft tissues of carcasses after approximately 1 week and bone marrow of infected animals after longer periods.
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Transfer of
bacteria to humans has also been reported from bites/scratches/
abscesses of infected domestic pets.
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Wild rodents are the natural
reservoir;
lagomorphs and carnivores may be a source of infection to humans.
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Since vaccination of free-ranging wildlife is not possible, large-scale attempts to control plague in both humans and endangered wildlife populations are directed mainly at eliminating flea populations – however, removal of non-target
insect species with associated ramifications to ecosystems have made this control method problematic.
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Removal of food sources and rodent habitats in areas occupied by humans will help to reduce rodent infestation and subsequently flea populations.
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Treatment of pets for fleas should also help to reduce transmission to humans and other wildlife.
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No control measures have ever been required in British Columbia as the level of plague appears to be low.
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Samples for Diagnosis |
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Appropriate personal protection should be used:
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eye protection, gloves, gowns, high-density surgical masks or respirators
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Plague suspects should be dusted with carbamate or pyrethrin insecticides to kill fleas.
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Using appropriate personal protection, collect a representative sample of fleas (mature, immature, male, female) of fresh, affected mammals.
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DO NOT ATTEMPT TO COLLECT TISSUE SAMPLES.
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Animals surviving infection with Y. pestis develop serum antibodies that can be used for diagnosis of exposure.
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Detection of antibodies in the blood of carnivores has been used to monitor plague activity in areas where plague is normally found.
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Similar Diseases |
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Acute
bacterial infections, such as
tularemia can mimic infection with Y. pestis.
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Both infections cause an
acute, feverish disease in certain species and can be followed by
pneumonia or sudden death.
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Also found in colonial rodents,
tularemia does not appear to induce the high mortality typical of plague.
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Infection with Pasteurella spp. bacteria may cause individual mortality in rodents and occasional localized die-offs.
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White spots or “spotty”
necrosis of the liver and spleen, observed in Y. pestis infection, can appear similar to other Yersinia sp. infections or may result from migration tracts of
parasites.
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Poisonings from rodenticides may also cause
acute population declines in colonial rodents.
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Further Reading |
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Gasper, P. W., and R. P. Watson. 2001. Plague and Yersiniosis. Pp. 313-329 in E. S. Williams and I. K. Barker (eds.), Infectious Diseases of Wild Mammals. 3rd Ed. Iowa State University Press, Ames, IA.
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